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case records of the massachusetts general hospital

Founded by Richard C. Cabot

Nancy Lee Harris, m.d., Editor Eric S. Rosenberg, m.d., Associate Editor
Jo-Anne O. Shepard, m.d., Associate Editor Alice M. Cort, m.d., Associate Editor
Sally H. Ebeling, Assistant Editor Christine C. Peters, Assistant Editor

Case 28-2007: A 68-Year-Old Man

with Syncope
James L. Januzzi, Jr., M.D., Joseph M. Garasic, M.D., Tomas G. Neilan, M.D.,
R. Gilberto Gonzalez, M.D., Ph.D., and James R. Stone, M.D., Ph.D.

Pr e sen tat ion of C a se

A 68-year-old man was admitted to this hospital because of a syncopal episode, fol- From the Coronary Care Unit (J.L.J.), Cardi-
lowed by hemiparesis and altered mental status. ology Division (J.L.J., J.M.G., T.G.N.), Vas-
cular Medicine Section (J.M.G.), and the
The patient was in his usual state of health until the morning of admission, when Departments of Medicine (J.L.J., J.M.G.),
he suddenly lost consciousness and vomited while walking with a companion. He was Radiology (R.G.G.), and Pathology (J.R.S.),
transferred by ambulance to the emergency department of another hospital with- Massachusetts General Hospital; and the
Departments of Medicine (J.L.J., J.M.G.,
in 35 minutes after the onset of symptoms. T.G.N.), Radiology (R.G.G.), and Pathology
On arrival, he said he did not have chest pain or headache, but he was unable to (J.R.S.), Harvard Medical School.
provide other history. On examination, he was lethargic, with intermittent periods of
N Engl J Med 2007;357:1137-45.
unresponsiveness. The blood pressure was 166/80 mm Hg, the pulse 74 beats per Copyright 2007 Massachusetts Medical Society.
minute, and the axillary temperature 36.1C; the respirations were 18 breaths per
minute. His gaze was deviated to the right, and he had a right facial droop and dif-
ficulty swallowing oral secretions. The patients left arm was flaccid, but he was able
to move his other limbs. There was no sign of head trauma; the remainder of the
examination was normal. The hematocrit was 30.6%, and the remainder of the com-
plete blood count was normal. The blood glucose level was 141 mg per deciliter (7.8
mmol per liter), and the potassium level 3.1 mmol per liter. Levels of other electro-
lytes, renal function, and liver function were normal. Urinalysis revealed dark-yel-
low, turbid fluid with a pH of 7.0, a specific gravity of 1.020, and a urobilinogen
level of 4.0 Erlich units per deciliter; the urine was positive for protein (2+), ketones
(3+), blood (1+), and esterase (3+). A radiograph of the chest showed pulmonary
vascular prominence with no evidence of edema, infiltrate, or effusion. An electro-
cardiogram revealed sinus tachycardia with ST-segment elevation in leads V3 through
V5. Tests for creatine kinase and troponin T were negative.
In the emergency department, the trachea was intubated orally for airway protec-
tion, and a nasogastric tube was placed. Computed tomographic (CT) scanning of the
head revealed right frontal and left cerebellar infarcts that appeared old, without evi-
dence of bleeding, edema, or midline shift. CT scanning of the chest and abdomen,
performed with the administration of contrast material, showed patchy perfusion of

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 The n e w e ng l a n d j o u r na l
the left kidney and no perfusion of the right kid-
ney. There was variable enhancement of the
small-bowel loops and a defect in the superior
mesenteric artery, findings that were consistent
with the presence of an embolus. After the in-
tubation procedure, morphine sulfate (2 mg)
was administered intravenously for agitation and
was repeated without benefit. Aspirin was ad-
ministered through the nasogastric tube, and
heparin (5000 U) was given intravenously. The
patient was transferred by ambulance to the emer-
gency department of this hospital 2hours after
the onset of symptoms.
The patient had a history of diabetes mellitus,
hypertension, and anemia. Four months before
admission, a diagnosis of prostatic carcinoma had
been made on transurethral prostatectomy. Che-
motherapy and radiation therapy were adminis-
tered, and a radical prostatectomy was planned
because of increasing levels of prostate-specific
antigen. The patient was allergic to penicillin.
Medications included rosiglitazone, glipizide, met-
formin, erythropoietin, goserelin, ketoconazole,
an amlodipine and benazepril combination, and
hydrocortisone. He lived with his wife and did
not smoke or drink alcohol.
On examination, the patient was observed to
be a thin man who was intubated, sedated, and
lethargic, responding to noxious stimuli by par-
tially opening his eyes. He did not withdraw when
pinched and did not follow commands. His blood
pressure was 182/78 mm Hg, and his pulse 93
beats per minute; respirations were by mechani-
cal ventilation. There were bilateral breath sounds
with a grade 2/6 holosystolic murmur radiating
from the left lower sternal border to the apex;
the abdomen was soft and was not distended.
The patients pupils were midline, equal, and slug-
gishly reactive, with a positive dolls-eye sign and
conjugate gaze. His face was symmetric; there was
minimal spontaneous limb movement, and the
muscles had normal tone. The remainder of the
examination was normal.
Arterial blood gas measurements while the
patient was breathing 100% oxygen revealed a
partial pressure of oxygen of 205 mm Hg and a
partial pressure of carbon dioxide of 35 mm Hg,
with a pH of 7.39. The hematocrit was 35%, the
prothrombin time 15.9 seconds (reference range,
11.1 to 13.1), and the partial-thromboplastin time
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of m e dic i n e
greater than 150 seconds (reference range, 22.1
to 35.1). The blood glucose level was 212 mg per
deciliter (11.8 mmol per liter), potassium 3.4 mmol
per liter, and serum creatinine 1.5 mg per decili-
ter (132.6 mol per liter). Tests for creatine ki-
nase MB isoenzymes and troponin T were nega-
tive, as was a test for occult blood in the stool.
Electrocardiography revealed ST-segment eleva-
tions in leads II, III, aVF, and V3 through V6.
Chest radiography showed endotracheal and na-
sogastric tubes in place and a small right pleu-
ral effusion, with left retrocardiac and midlung
opacities that may have represented atelectasis,
pneumonia, or effusion and moderate pulmonary
edema.
Transthoracic echocardiography showed hypo-
kinesis of the anterior, septal, and apical walls of
the left ventricle. Overall left ventricular systolic
function was at the lower limit of the normal
range. There was incomplete closure of the pos-
terior mitral-valve leaflet and an associated jet of
mild-to-moderate mitral regurgitation. The left
atrium was dilated. There was a mobile echoden-
sity in the left atrium that was attached to or as-
sociated with the atrial septum. Subsequent trans-
esophageal views revealed a mass, 2.3 cm by
1.5 cm, with its base attached to the interatrial
septum. The mass was highly mobile and con-
tained multiple frondlike elements. Color Doppler
imaging showed no evidence of a patent foramen
ovale.
Magnetic resonance imaging (MRI) of the brain
revealed multiple punctate and confluent new in-
farcts in the bilateral occipital and frontal lobes,
the cerebellum, and the right temporal lobe, as
well as old encephalomalacia in the left cerebel-
lum. There was no perfusion delay.
Interventional angiography performed approx-
imately 5 hours after the onset of symptoms re-
vealed an occlusive filling defect in the distal left
anterior descending coronary artery. Balloon dila-
tion improved filling, but there was a persistent
occlusion in the distal apical segment of the ves-
sel. Arterial occlusions were also found in branch-
es of both renal arteries, resulting in obstruction
of flow to the top third of the right kidney and the
middle third of the left kidney. The superior mes-
enteric artery was completely occluded proximally
by what appeared to be an embolus. Multiple at-
tempts at catheter-based embolectomy of the supe-
 case records of the massachuset ts gener al hospital
rior mesenteric artery and local administration of
tissue plasminogen activator (a 5-mg pulse deliv-
ered intraarterially) were unsuccessful in restoring
flow. Small amounts of gelatinous material were
removed and sent for pathological examination.
Six hours after admission, the aspartate ami-
notransferase level was 130 U per liter (normal
range, 0 to 35), and the amylase level was 118 U
per liter (normal range, 3 to 100). Measurements
of cardiac enzymes revealed a creatine kinase level
of 810 U per liter, a creatine kinase MB isoenzyme
level of 133.4 ng per milliliter, a creatine kinase MB
index of 16.5%, and a troponin T level of 4.09 ng
per milliliter.
A diagnostic procedure was performed.
Differ en t i a l Di agnosis
Dr. James L. Januzzi, Jr.: May we review the imaging
studies?
Dr. R. Gilberto Gonzalez: MRI restricted to diffu-
sion-weighted and perfusion-weighted imaging
was performed in the emergency department of
this hospital. Diffusion-weighted images show
numerous foci of abnormal hyperintense signal
throughout the brain, involving all the vascular
distributions (Fig. 1A). The largest abnormalities
were seen in the right occipital lobe and the left
frontal lobe. Apparent-diffusion-coefficient im-
ages confirmed that these lesions had reduced
water diffusion and were consistent with acute
ischemic infarctions. The distribution of the le-
sions suggested an embolic pattern. Perfusion-
weighted images demonstrated that the abnor-
malities of cerebral blood flow (Fig. 1B) matched
the abnormalities on the diffusion-weighted im-
ages. The distribution and pattern of these lesions
suggest an embolic source proximal to the great
vessels of the neck.
Dr. Tomas G. Neilan: Both transthoracic and trans-
esophageal echocardiograms were obtained. There
was an area of hypokinesis involving the antero-
septal wall of the left ventricle; the overall left
ventricular systolic function was preserved, and
there was no visible left ventricular thrombus. In
the left atrium, adjacent to the interatrial septum,
there is a mobile echodensity measuring 1.3 by
1.5 cm (Fig. 2). The mass has a broad base, with
multiple frondlike elements, and is attached to the
interatrial septum, close to the fossa ovalis. No
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evidence of a patent foramen ovale could be de-
tected on color Doppler imaging.
Dr. Joseph M. Garasic: Angiography of the left an-
terior descending coronary artery shows sluggish
flow and an apical filling defect (Fig. 3A). The
distal left anterior descending artery was treated
with balloon angioplasty, but there was little
change in the appearance of the occluded seg-
ment. Visceral angiography was then performed.
Selective angiography of the right renal artery
shows an occluded subbranch of the right supe-
rior renal artery and mobile filling defects in the
main right renal artery, with no opacification of
the apical segment of the nephrogram of the
right kidney, all of which suggest the presence
of emboli (Fig. 3B). Angiography of the left renal
artery also demonstrated occlusion of multiple
distal subbranches, a finding consistent with the
presence of emboli.
Selective angiography of the superior mesen-
teric artery demonstrates proximal occlusion of the
vessel (Fig. 3C). The occluded superior mesenteric
artery was treated with balloon angioplasty, re-
combinant tissue plasminogen activator, and at-
tempts at catheter-based embolectomy, with little
improvement in antegrade flow. A filter-type de-
vice was placed beyond the site of total occlusion
in a final attempt at embolectomy of the superior
mesenteric artery, and a small amount of gelati-
nous material was recovered and sent for patho-
logical examination. Because of our inability to
restore flow, further attempts at catheter-based
embolectomy were abandoned.
Dr. Januzzi: This patient with a history of carci-
noma of the prostate and hypertension presented
with abrupt syncope, multifocal neurologic defi-
cits, a murmur of mitral regurgitation, and evi-
dence of an acute myocardial infarction. Although
the differential diagnosis for syncope in a patient
with myocardial infarction includes ventricular ar-
rhythmia, the history and physical examination
indicate that arrhythmia was probably not the
cause of his loss of consciousness. A neurologic
cause is more likely, and cerebral imaging sug-
gests that the syncope was probably the result of
emboli to the brain. In addition to his cerebral le-
sions, the patient had multiple embolic lesions in
the vasculature of the heart, kidneys, and gut.
Given the echocardiographic findings, we must
therefore consider the differential diagnosis of car-
1139
 The n e w e ng l a n d j o u r na l of m e dic i n e

A A

Figure 2. Transthoracic and Transesophageal Echocar-

diograms.
ICM AUTHOR Januzzi RETAKE 1st
REG F FIGURE fig 2 a,b 2nd
A transthoracic echocardiogram shows an apical, four- 3rd
CASE TITLEof the heart. Panel A shows the
chamber view left
Revised ven-
EMail Line left atrium
4-C
tricle (LV), right ventricle (RV), (LA), right
Enon ARTIST: mleahy SIZE
atrium (RA), and interatrial H/T H/T (see also
septum (IAS)
FILL Combo 16p6
Video 1 in the Supplementary Appendix, available with
AUTHOR,
the full text of this article PLEASE NOTE:
at www.nejm.org). A poorly
Figure has been redrawn and type has been reset.
circumscribed mass (arrow) appears
Please check carefully. to be adjacent to
the interatrial septum. A transesophageal view (Panel B)
showsJOB:the 35711
left atrium, right atrium, and interatrial
ISSUE: 09-13-07 sep-
tum. A poorly circumscribed mass (arrow) is attached
Figure 1. MRI Scans of the Brain. to the interatrial septum in the left atrium. The mass
ICM AUTHOR
Diffusion-weighted Januzzi
images
RETAKE
of the brain show multifo-
1st
2nd
measures 1.5 by 1.3 cm. AV denotes aortic valve.
REG F FIGURE
cal hyperintense signal abnormalities in all vascular3rd
CASE TITLE
distributions of the anterior and posterior cerebral
Revised cir-
EMail
culations. The abnormalitiesLine 4-C
were confirmed to
SIZE
reflect
Enon
restrictionARTIST:
of watermleahy
diffusionH/T H/T
on the corresponding
16p6 ap-
Infectious Causes of Cardiac-Based Embolism
FILL Combo
Infective endocarditis is always a possibility when
parent-diffusion-coefficient image (Panel A). Corre-
sponding perfusion AUTHOR, PLEASE
imaging NOTE:
shows that the abnormali-
a patient presents with multiple peripheral em-
Figure has been redrawn and type has been reset.
ties of perfusion matched thecarefully.
Please check diffusion abnormalities
(Panel B). The appearance is most consistent with
boli, particularly when they are accompanied by a
acute ischemic
JOB: 35711infarctions due to multiple
cardiac murmur on physical examination. This pa-
emboli.
ISSUE: 09-13-07
tient had hematuria, which in the setting of infec-
tive endocarditis may occur with or without renal
diac sources of embolism. I will focus on the three failure due either to involvement of the kidney by
most likely diagnostic categories: infective endo- infectious emboli or to immune-complex deposi-
carditis, intracardiac thrombus, and cardiac neo- tion. However, this patient did not have other pe-
plasm. ripheral stigmata of endocarditis, such as Oslers

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 case records of the massachuset ts gener al hospital

nodes or Janeways lesions, splinter hemorrhages

in the nail beds, or proliferative retinal lesions. Al- A
though endocarditis may present as a cardiac mass,
such presentations are usually related to a precipi-
tating cause, such as an infected catheter project-
ing into the right atrium,1 which was not present
in this case. It would also be unusual for endocar-
ditis to present with no systemic symptoms, such
as fever or malaise, or evidence of inflammation,
such as leukocytosis or an elevated erythrocyte sed-
imentation rate.

Thrombotic Causes of Cardiac-Based

Embolism
Peripheral embolization of intracardiac thrombus
is an important consideration in this case. Throm-
bus is the most common cause of an intracardiac B
mass, and these masses may have diverse appear-
ances in imaging studies and may mimic a neo-
plastic process.2-5
Most cardiac thrombi are formed as a conse-
quence of abnormalities, such as stasis, injury, or
hypercoagulability. This patient presented with a
myocardial infarction at the anterior wall, and
mural thrombi form in many patients with ante-
rior myocardial infarction.6,7 However, the ante-
rior-wall infarction does not explain the mass in
the atrium, and this patient does not have typi-
cal risk factors for atrial thrombosis, such as mi-
tral-valve stenosis or atrial fibrillation.
C
Another cause of intracardiac thrombus that
should be considered is nonbacterial thrombotic
endocarditis, a diagnosis most often associated
with advanced cancers or the antiphospholipid
syndrome. Nonbacterial thrombotic endocarditis
typically presents with valvular lesions, which may
be progressive and destructive of the valve tissue
and in many ways may resemble infective endocar-
ditis.8-10 The lesion in the patients atrium, how-
ever, is not characteristic of this condition.
In this case, the location of the mass at the site
of the fossa ovalis may be an important clue. The
fossa ovalis is an indentation of the atrial septum Figure 3. Coronary and Visceral Angiograms.
that represents the remains of the foramen ovale, A left coronary angiogram (Panel A) shows occlusion
a channel connecting the left and right atria in of the
ICMdistalAUTHOR Januzzi
left anterior descending artery (arrow).1st
RETAKE On
intrauterine life. In the majority of people, the fora- selective
REG F angiography
FIGURE Fig 3 a,b,c,
of the right renal artery (Panel 2nd
3rd
men ovale closes after birth, but in up to 27% of B), CASE
there isTITLE
no opacification of the apical segment
Revised
(ar-
EMail
rows) of the nephrogram ofLine the right4-C
kidney, as a result
people, the foramen ovale is patent,11 potentially Enon
of embolic occlusion. Selective ofSIZE
ARTIST: mleahy H/T angiography
H/T the su-
allowing a thromboembolism from the venous FILL Combo 16p6
perior mesenteric artery (Panel C) shows total proxi-
circulation to pass to the systemic circulation mal occlusion (arrow)
AUTHOR,of the vessel.
PLEASE (See also Videos 2,
NOTE:
rather than traveling to the lungs. This finding is 3, and Figure hasSupplementary
4 in the been redrawn andAppendix.)
type has been reset.
Please check carefully.
important to consider in patients with unexplained
JOB: 35711 ISSUE: 09-13-07

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 The n e w e ng l a n d j o u r na l of m e dic i n e

not been reported to metastasize to the heart are

Table 1. Common Cardiac Tumors.
Primary Tumors of the Heart Tumors Metastasizing to the Heart*
Malignant tumors Melanoma
Pheochromocytoma Lung tumors (may spread hematogenously
and paraganglioma or invade directly from an adjacent struc-
tures)
Mesothelioma Breast tumors
Sarcoma Esophageal tumors
Lymphoma Lymphoma
Benign tumors Thyroid tumors
Hamartoma Lower gastrointestinal carcinomas
Lipoma Renal-cell tumors
Fibroma Uterine tumors
Rhabdomyoma Endometrial or ovarian tumors
Hemangioma Prostate tumors
Dermoid tumors
Papillary fibroelastoma
Myxoma
* Metastatic tumors of the lower gastrointestinal tract, the kidney, the uterus,
the endometrium and the ovaries, and the prostate may invade the heart
through the vena cava.
cardioembolic stroke. This mass could represent
the entrapment of a thrombus in transit within a
patent foramen ovale. We are told that the foramen
ovale was not patent, and in view of the poor re-
sponse of the emboli to therapies for thrombus,
as well as the gross appearance of the embolec-
tomy specimen, a diagnosis of thrombus seems
unlikely, leaving the possibility of an intracardiac
neoplasm arising in the area of the fossa ovalis.
Neoplastic Causes of Cardiac-Based Embolism
Metastatic tumors in the heart (Table 1) are at least
40 times as common as primary cardiac tumors;
a metastatic tumor is thus an important consid-
eration in this patient, who has a history of can-
cer and a cardiac mass. Cardiac metastases involve
the pericardium, epicardium, and myocardium, in
decreasing order of frequency. Endocardial metas-
tases, which are rare, typically occur either by ex-
tension from the vena cava or pulmonary veins or
by direct invasion of the heart from adjacent ar-
eas such as the lungs. The only tumors that have
tumors of the central nervous system. However,
certain malignant tumors have a predilection for
the heart, including cancers of the lung, breast,
thyroid, kidney, and esophagus; melanomas; and
lymphomas. This patient has prostate cancer; al-
though malignant tumors of the genitourinary sys-
tem may affect the heart, it is particularly rare for
carcinoma of the prostate to do so. Finally, cardiac
metastases are typically multiple and clinically si-
lent. I was unable to find a report of a solitary car-
diac metastasis involving the interatrial septum
of the heart. Since it is unlikely that this mass is
due to metastatic prostate cancer, a primary car-
diac neoplasm is the most probable diagnosis
(Table 1).
Primary Cardiac Tumors
The great majority of primary cardiac tumors are
histologically benign. Although malignant primary
tumors of the heart may present as intracardiac
lesions, much like the lesions in this patient, they
are extremely rare, and this patient did not have
the typical findings of an aggressive malignant
condition, including constitutional symptoms.
Although benign tumors of the heart are rare
autopsy studies suggest that the overall preva-
lence is between 0.001 and 0.25% of the popula-
tion12 it is estimated that they account for more
than 75% of primary tumors of the heart. Al-
though these tumors do not metastasize, they can
have catastrophic effects due to impairment of
cardiac structure and function, including the pre-
cipitation of arrhythmias or embolism.
Fibromas may be found within the cardiac
chambers, often involving the valves, but they do
not typically have the features described in this
case and are reported to have a low potential for
embolization. Extraadrenal pheochromocytoma,
or paraganglioma, may present as intracardiac
masses, but these tumors are frequently accompa-
nied by hypertension, flushing, and tachycardia.
Papillary fibroelastoma is an important consider-
ation in this case, since these benign cardiac tu-
mors may have a frondlike appearance and they
have a high likelihood of embolization. Although
papillary fibroelastomas typically arise from car-
diac valves, they may arise from the endocardium

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 case records of the massachuset ts gener al hospital
of the cardiac chambers and in one reported case
were found to arise from the interatrial septum.13
The clinical features of this case are most typi-
cal of myxoma, which is the most common be-
nign primary tumor of the heart, accounting for
up to 50% of primary cardiac tumors. The ma-
jority of myxomas are solitary and occur in the left
atrium, typically in the zone of the fossa ovalis,
as in this case. When multiple, recurrent, ventricu-
lar, or familial myxomas are discovered, there is
cause to consider the diagnosis of Carneys syn-
drome, a familial syndrome characterized by mul-
tiple neoplasms.14
The clinical features of atrial myxoma vary, and
the diagnosis is often incidental. Symptoms in-
clude dizziness, syncope, and dyspnea and are
usually caused by intermittent obstruction of the
mitral valve by a prolapsing tumor. In up to 50%
of cases, cytokine production by the tumor may
result in fever, weight loss, arthralgias or myalgias,
and Raynauds phenomenon.15 Embolism occurs
in 30 to 40% of cases and may result from in-
fected or uninfected thrombi on the tumor or from
the release of fragments of the tumor itself. Em-
bolization of tumor fragments is probably the
cause of this patients problems.
Physical findings may include elevated jugular
venous pressure related to failure of the right side
of the heart, a loud S1 with or without a loud P2,
and a diastolic rumble, due to mitral-valve obstruc-
tion; a tumor plop a diastolic filling sound
may also be noted. This patient had no specific
cardiac findings on examination.
Myxomas are notoriously difficult to diagnose.
The current tests of choice are echocardiography
and cardiac MRI with gadolinium injection, which
is useful to distinguish tumor from thrombus be-
cause tumors are typically enhanced with gado-
linium, whereas thrombi are not.
My diagnosis is a left atrial myxoma, presum-
ably with a grossly villous appearance, complicated
by emboli to the cerebral, coronary, renal, and
mesenteric territories. I expect that the diagnostic
procedure consisted of analysis of the embolecto-
my tissue, followed by prompt cardiac surgical re-
moval of the atrial tumor.
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Cl inic a l Di agnosis
Anterior myocardial infarction and occlusion of the
renal and mesenteric arteries resulting from em-
bolization of a left atrial myxoma.
DR . JA ME S L . JA NUZ ZI, jr .S
DI AGNOSIS
Left atrial myxoma, with embolization to the cere-
bral, coronary, renal, and mesenteric vasculature.
Pathol o gic a l Dis cus sion
Dr. James R. Stone: Open embolectomy of the supe-
rior mesenteric artery and the left and right com-
mon femoral arteries was performed. Histologi-
cally, the embolectomy specimens all showed
spindle-to-polygonal cells, with oval nuclei form-
ing multinucleated syncytia within a proteoglycan-
rich myxoid matrix, admixed with variable amounts
of fibrin (Fig. 4A). Immunohistochemistry showed
that the cells were strongly positive for calretinin,
a calmodulin-like calcium-binding protein of un-
known function (Fig. 4B). Normal endocardium
and organizing thrombi do not stain for calretinin,
whereas 80 to 100% of cardiac myxomas show
strong staining for this marker.16 These histologic
features are diagnostic of cardiac myxoma.16,17
Subsequently, surgical resection of the left atrial
mass was performed and the atrial septum repaired
with a pericardial patch. The resected mass was
1.7 cm in diameter, with an irregular frondlike sur-
face (Fig. 4C and 4D). On microscopical examina-
tion, the mass also had the morphologic features
of a cardiac myxoma.
Dr. Rosenberg: The patient was discharged to
a rehabilitation hospital and then to a nursing
home. He had persistent cognitive defects, poor
memory, persistent weakness and neglect of the
left side, and possible ongoing seizure activity. He
had episodes of Clostridium difficile colitis, conges-
tive heart failure, and chronic renal insufficiency,
requiring several readmissions to this hospital. He
died 8 months after his initial admission to this
hospital.
1143
 The n e w e ng l a n d j o u r na l of m e dic i n e

A B

C D

Figure 4. Embolectomy Specimen from the Superior Mesenteric Artery and Resected Left Atrial Tumor.
A section of an embolus (Panel A) shows spindle-to-polygonal myxoma cells with oval nuclei, forming multinucleat-
ed syncytia within a myxoid matrix. ICM AUTHOR
Immunohistochemical Januzzi RETAKE
testing for calretinin 1st
(Panel B) shows strong staining of
fig 4myxoma
a_d 2nd
the myxoma cells. A low-power viewREG of FtheFIGURE
resected left atrial shows a mass 3rd
with an irregular, frondlike
CASE TITLE (Panel C). A higher-power view
surface attached to a segment of atrial septum of the irregular surface of the myxo-
Revised
EMail Line
ma shows frondlike structures with adherent fibrin thrombus (Panel4-C
D). (Panels A, C, and D, hematoxylin and eo-
Enon ARTIST: mleahy SIZE
sin; Panel B, immunoperoxidase stain for calretinin.) H/T H/T
FILL Combo 33p9
AUTHOR, PLEASE NOTE:
Figure has been redrawn and type has been reset.
Please check carefully.

A nat omic a l Di agnosis

JOB: 35711 ISSUE: 9-13-07
Four videos showing an echo
Left atrial cardiac myxoma with systemic emboli- cardiogram of the patients
zation. heart and angiograms of
Dr. Januzzi reports receiving consulting fees from Roche Di- affected arteries are available
agnostics and Dade-Behring; lecture fees from Dade-Behring, with the full text of this article
Ortho Clinical Diagnostics, Biosite, and Roche Diagnostics; and
at www.nejm.org.
grant support from Roche and Inverness Medical. Dr. Garasic
reports receiving lecture fees from Bristol-Myers Squibb and
Sanofi-Aventis. Dr. Stone reports receiving consulting fees from
Merck, MuscleTech, GNC, and Wal-Mart. No other potential
conflict of interest relevant to this article was reported.

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